A recent major finding of this work has been the definition of marked differences between the responses of adult and fetal-neonatal Leydig cells to gonadotropic stimulation. The adult-type Leydig-cell response is that of initial stimulation of receptor expression and steroidogenesis, followed by a prominent phase of LH and prolactin receptor loss or down-regulation, and of refractoriness to further hormonal stimulation. The latter effect involves both desensitization at the cell-membrane level and steroidogenic defects that result from estrogen-dependent inpairment of androgen biosynthetic enzymes. In the fetal-neonatal testis, only the stimulatory actions of LH or hCG are manifested, with none of the receptor loss and desensitization that is characteristic of the adult testis. This absence of steroidogenic lesions in the fetal Leydig cell could result from the lack of estrogen production and/or receptors in early development, whereas the absence of receptor down-regulation could reflect differences in receptor-ligand binding kinetics and/or receptor turnover in the immature testis. A further difference in receptor regulation has been observed in the lactogen receptors of the Leydig cell, which in the adult testis undergo marked but transient depletion during LH/hCG stimulation. In immature rats, the lactogen receptors were increased after gonadotropin stimulation, and did not show the adult-type decrease until 30-40 days of age. The analysis of gonadotropin receptor regulation and steroidogenic responses in cultured embrionic rat testes also revealed that the fetal Leydig cell lacks the gonadotropin receptor loss and desensitization that occur in the adult testis, and provides an in vitro system for the further investigation of this development difference. The ontogeny of gonadotropin receptors was studied during fetal and neonatal development in the rat, and revealed a progressive rise in LH sites from day 15.5, when biological responses to the hormones are first detectable. FSH sites appeared at 17.5 days and remained low until 20.5 days, rising just before birth in a manner consistent with a functional role of FSH in the late fetal and early neonatal development of the testis.